Spinal origin of sympathetic preganglionic neurons in the rat

Strack, Alison M.; Sawyer, William; Marubio, Lisa M.; Loewy, A.

doi:10.1016/0006-8993(88)90132-1

Cited by 325 publications

(222 citation statements)

References 8 publications

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“…The distribution of cells in the thoracic spinal cord from the adrenal injections closely matched that seen by Strack et al (1988Strack et al ( , 1989 in similar experiments with a peak concentration in thoracic segments 6 -9. No infected cells were observed in cervical cord.…”

Section: Resultssupporting

confidence: 75%

GABAergic Neurons in the Central Region of the Spinal Cord: A Novel Substrate for Sympathetic Inhibition

Deuchars¹,

Milligan²,

Stornetta³

et al. 2005

J. Neurosci.

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Homeostatic maintenance of widespread functions is critically dependent on the activity of the sympathetic nervous system. This activity is generated by the CNS acting on the sole output cells in the spinal cord, sympathetic preganglionic neurons (SPNs). SPNs are subject to control from both supraspinal and spinal inputs that exert effects through activation of direct or indirect pathways. A high proportion of indirect control is attributable to activation of spinal interneurons in a number of locations. However, little is known about the different groups of interneurons with respect to their neurochemistry or function. In this study, we report on a novel group of GABAergic interneurons located in the spinal central autonomic area (CAA) that directly inhibit SPN activity. In situ hybridization studies demonstrated a group of neurons that contained mRNA for glutamic acid decarboxylase (GAD) 65 and GAD 67 within the CAA. Combining in situ hybridization with trans-synaptic labeling from the adrenal gland using pseudorabies virus identified presympathetic GABAergic neurons in the CAA. Electrical stimulation of the CAA elicited monosynaptic IPSPs in SPNs located laterally in the intermediolateral cell column. IPSPs were GABAergic, because they reversed at the chloride reversal potential and were blocked by bicuculline. Chemical activation of neurons in the CAA hyperpolarized SPNs, an effect that was also bicuculline sensitive. We conclude that the CAA contains GABAergic interneurons that impinge directly onto SPNs to inhibit their activity and suggest that these newly identified interneurons may play an essential role in the regulation of sympathetic activity and thus homeostasis.

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Section: Resultssupporting

confidence: 75%

GABAergic Neurons in the Central Region of the Spinal Cord: A Novel Substrate for Sympathetic Inhibition

Deuchars¹,

Milligan²,

Stornetta³

et al. 2005

J. Neurosci.

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“…The effect of 2DG on Fos expression in the latter cord regions was quite selective, with expression in other regions not exceeding control levels. This distribution of immunoreactive nuclei strongly indicates a selective activation by 2DG of adrenal medullary preganglionic neurons, since these are located in the IML at cord levels T5-Tl2, with a concentration in T7-TlO (28). In contrast to ZDG, MA did not increase Fos-li in either the adrenal medulla or the IML.…”

Section: Resultsmentioning

confidence: 68%

2‐Deoxy‐D‐Glucose but not 2‐Mercaptoacetate Increases Fos‐Like Immunoreactivity in Adrenal Medulla and Sympathetic Preganglionic Neurons

1995

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2-Deoxy-D-glucose (2DG) and 2-mercaptoacetate (MA) are drugs that competetively inhibit metabolism of glucose and fatty acids, respectively. Both 2DG and MA stimulate food intake. In addition, 2DG-induced glucoprivation is a known stimulus for adrenomedullary secretion. However, very little is known about the effects of MA on the sympathoadrenal system. In the present study, we examined effects of 2DG and MA on the activity of preganglionic neurons and the adrenal medulla, as indicated by expression of Fos-like immunoreactivity (Fosli). 2DG, MA, or saline was administered using a stress-attenuated paradigm incorporating remote drug infusion. Expression of Fos-like immunoreactivity (Fos-li) was subsequently examined in the adrenal medulla and in preganglionic sympathetic neurons throughout the intermediolateral column (IML) of the thoracic and lumbar spinal cord. We found that 2DG increased Fos-li in the adrenal medulla and in the IML primarily a t spinal cord segments T7-Tl0, where adrenomedullary preganglionic neurons reside. In contrast, MA did not induce Fos-li either in the adrenal medulla or in sympathetic preganglionic neurons a t any cord level. Results support the hypothesis that decreased fatty acid oxidation is not a stimulus for adrenal medullary secretion and provide evidence for a highly selective stimulation of adrenal medullary preganglionic neurons by 2DG.

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“…PRV-Bartha is likely to reach this tissue solely via through retrograde spread within the GVA pathways. It is noteworthy that visceral organs are only sparsely innervated by GVA neurons, further accounting for the lower levels of PRVBartha detected (26).…”

Section: Distinctive Symptoms Of Virulent Prv Flank Infectionmentioning

confidence: 94%

“…Infection reaches these organs either (i) by anterograde spread along sympathetic neurons from the lumbar or thoracic spinal cord, (ii) by parasympathic neurons running from lumbar spinal segments through the inferior mesenteric ganglion, or (iii) by retrograde spread from the general visceral afferent (GVA) pathways that connect the lumbar spinal cord and the bladder, adrenal glands, and kidneys. These routes of infection in rodents are well characterized (26). In contrast, the only tissues from PRV-Bartha-infected mice yielding even modest titers of infectious virus were the adrenal glands.…”

Section: Distinctive Symptoms Of Virulent Prv Flank Infectionmentioning

confidence: 99%

Two Modes of Pseudorabies Virus Neuroinvasion and Lethality in Mice

Brittle

Reynolds

Enquist

2004

J Virol

123

142

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We describe two distinct modes of neuroinvasion and lethality after murine flank inoculation with virulent and attenuated strains of pseudorabies virus (PRV). Mice infected with virulent (e.g., PRV-Becker, PRVKaplan, or PRV-NIA3) strains self-mutilate their flank skin in response to virally induced pruritus, die rapidly with no identifiable symptoms of central nervous system (CNS) infection such as behavioral abnormalities, and have little infectious virus or viral antigen in the brain. In distinct contrast, animals infected with an attenuated PRV vaccine strain (PRV-Bartha) survive approximately three times longer than wild-type PRVinfected animals, exhibit severe CNS abnormalities, and have an abundance of infectious virus in the brain at the time of death. Interestingly, these animals have no skin lesions and do not appear pruritic at any time during infection. The severe pruritus and relatively earlier time until death induced by wild-type PRV infection may reflect the peripheral nervous system (PNS) and immune responses to infection rather than a fatal, virally induced CNS pathology. Based on previously characterized afferent (sensory) and efferent (motor) neuronal pathways that innervate the skin, we deduced that wild-type virulent strains transit through the PNS via both afferent and efferent routes, whereas PRV-Bartha travels by only efferent routes in the PNS en route to the brain.Pseudorabies virus (PRV), a swine alphaherpesvirus, is a member of the alphaherpesvirus subfamily, including human and animal pathogens such as varicella-zoster virus, herpes simplex virus type 1 (HSV-1) and HSV-2, bovine herpesvirus types 1 and 5, and equine herpesviruses types 1 and 4 (23). Although the natural hosts of PRV are adult swine, PRV is pantropic, infecting avian embryos and a wide range of mammalian species, with the notable exceptions of humans and other higher-order species of nonhuman primates.PRV routinely establishes a latent infection in PNS ganglia of adult swine and yet rarely invades the central nervous systems (CNS) of these animals (8). Viral spread between adult swine occurs primarily via direct mucosal contact. Common sequelae of wild-type PRV infection include respiratory disease, weight loss, and infertility in pregnant gilts and sows (31). In contrast, PRV infection is lethal in neonatal piglets and in nonnative hosts such as cows, dogs, rodents, and other susceptible animals. In these animals, infection induces severe, uncontrollable pruritus (itchiness), culminating in frantic selfmutilating behavior historically described as "mad itch." Death ensues within days of infection with virulent strains of PRV. The cause of death of these animals has traditionally been ascribed to fatal encephalitis.Adult swine infected with live, attenuated vaccine strains such as PRV-Bartha typically exhibit few, if any, symptoms of infection. In addition, most attenuated PRV strains are significantly less virulent in nonnative hosts such as rodents (8). Despite the attenuated phenotype, PRV-Bartha remains neuroinvas...

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Spinal origin of sympathetic preganglionic neurons in the rat

Cited by 325 publications

References 8 publications

GABAergic Neurons in the Central Region of the Spinal Cord: A Novel Substrate for Sympathetic Inhibition

GABAergic Neurons in the Central Region of the Spinal Cord: A Novel Substrate for Sympathetic Inhibition

2‐Deoxy‐D‐Glucose but not 2‐Mercaptoacetate Increases Fos‐Like Immunoreactivity in Adrenal Medulla and Sympathetic Preganglionic Neurons

Two Modes of Pseudorabies Virus Neuroinvasion and Lethality in Mice

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